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Nursing 272: Final Semester > Unit 1: Traumatic Brain Injury (TBI) > Flashcards

Unit 1: Traumatic Brain Injury (TBI) Flashcards

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1
Q

Traumatic Brain Injury (TBI)

A
  • can cause financial and human costs
  • many unable to return to previous roles in the family and in their personal and professional lives
  • care of the patient occurs best in environments where seamless continuity and progression of care can occur, from emergency medical services (EMS) to the emergency department (ED) to the operating room (OR), the critical care unit, acute care unit or facility, and outpatient services
  • classified by the Glasgow coma scale
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2
Q

Glasgow Coma Scale Score for TBI categories of injury

A

> Mild 13-15
Moderate 9-12
Severe = or < 8 (coma)

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3
Q

Coup

A

damage to the primary area of impact; primary injury; “blow”

  • shearing
  • twisting
  • diffuse axonal injury
  • blood vessel dissection
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4
Q

Contrecoup

A

damage sustained to the area opposite to impact; secondary injury; “counter blow”

  • contusion
  • swelling
  • blood clots
  • epidural and subdural hematoma
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5
Q

Primary Brain Injury

A

d/t the initial insult

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6
Q

Secondary Brain Injury

A

encompasses all processes that occur after the injury

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7
Q

Treatment protocols are aimed at what?

A

preventing or managing hypotension and hypoxemia in the immediate period after injury

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8
Q

Traumatic Brain Injury Types

A
  • Scalp Laceration
  • Skull Fractures (Open, Closed, Basilar)
  • Concussion
  • Contusion
  • Hematomas
  • Neuronal Injury
  • Vascular Injury
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9
Q

Open Skull Fracture

A
  • a disruption of the scalp such that the skull is exposed to the atmosphere
  • these bleed profusely d/t numerous blood vessels in close proximity to the scalp
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10
Q

Closed Skull Fracture

A
  • may be palpated through the scalp

- visualized on x-ray or other radiographical imaging

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11
Q

Basilar Skull Fractures

A
  • base of skull
  • carries additional risk of infection if there is evidence of CSF leak from the ears, nose, or sinus tract
  • late sign = bruising around the eyes (Racoon’s eyes) or ears (battle’s sign)
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12
Q

Epidural Hematoma

A

blood collects in the potential space between the skull and the dura mater

  • blood fills a particular epidural space and begins to compress or displace brain tissue inward, causing a concave appearance on radiographical imaging
  • when an artery is damaged flow of blood is very rapid and under pressure, speed with which blood collects and potential amount can cause rapid increase in ICP and herniation of brain tissue laterally then down if not stopped
  • epidural hematoma = neurosurgical emergency; requires prompt evacuation of blood clot and repair to damaged vessels
  • clinical manifestation: “talk and die” phenomenon
  • Tx: Burr holes to relieve pressure and evacuate the blood w/ cauterization of the artery
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13
Q

Clinical Presentation when there is an Epidural Hematoma

A
  • comatose state on initial presentation to a lucid (aware of surroundings) state, depending on size and location of hematoma as well as rate and volume of blood collection in epidural space
  • can initially loose consciousness, regain consciousness and appear lucid, and then very rapidly deteriorate to unresponsiveness w/ signs of cerebral herniation syndrome
  • “talk and die” phenomenon
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14
Q

Subdural Hematoma

A

collection of blood beneath the dura and above the arachnoid layer

  • can continue into brain tissue
  • the brain is connected to the inner surface of the dura by a network of veins called bridging veins; when head is impacted by a blunt force, the brain moves within the skull and dural covering; when brain moves, tension is placed on bridging veins = stretching and tearing, releasing a steady flow of blood around the brain in the subdural space, increasing ICP
  • symptoms appear over the course of hours or even a few days
  • Tx of neurosurgical intervention depends on clinical stability of the patient and state of neurological examination; based upon neurological exam; monitoring done if there are no motor deficits and patient is A&Ox3
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15
Q

Contusion

A

bruise on the surface of the brain that has the potential to transform into a hematoma

  • associated w/ development of cerebral edema
  • serial neurological assessments; evaluate for increased ICP
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16
Q

Concussion

A

injury w/ no findings with imaging but w/ damage at the cellular level d/t brain hitting inside of skull

  • LOC does not nee to occur
  • Symptoms: headache, amnesia, confusion, vertigo, inability to concentrate
  • Treatment: Brain rest
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17
Q

Neuronal Injury

A

Diffuse axonal injury (DAI)
-direct injury to neurons d/t shearing and rotational forces
-poor outcome
-MRI and PET scan help characterize the neuronal response to head injury
-severity depends on location and extent of injury
-swelling and microscopic hemorrhages can occur
>Sympathetic storming: sympathetic dysregulation; episodic tachycardia, tachypnea, and hyperthermia; spontaneous motor posturing (flexor or extensor)
-require supportive care of all systems in critical care setting
-require intubation and ventilatory support
-Tx: maintain ICP WNL; prevent complications
-coma often results

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18
Q

Vascular Injury

A

Traumatic Subarachnoid Hemorrhage (SAH): focal in location

  • diffuse layering of blood in the arachnoid layer
  • occurs as a result of disruption of veins and arteries transversing the arachnoid layer
  • local vasospasms
  • poor prognosis
  • care is supportive w/ cerebral edema commonly occurring
  • clot formation d/t the injury can occur; risk for stroke
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19
Q

Complications from Traumatic Brain Injury (TBI)

A
  • Increased ICP
  • Herniation Syndromes
  • Meningitis (w/ open fractures and dural tears)
  • Dural tears
  • Seizures (blood is irritant to brain tissue)
  • Diabetes Insipidus (d/t lack of ADH from pituitary)
  • Syndrome of Inappropriate diuretic hormone (SIADH) (excessive ADH from pituitary)
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20
Q

Complications: Diabetes Insipidus

A
  • symptoms: increased urinary output of dilute urine; hypernatremia; low urine specific gravity (<1.005)
  • when swelling in the brain places pressure directly on the posterior portion of the pituitary gland or on blood vessels supplying this area, disorders of sodium and water balance occur; antidiuretic hormone (ADH) is secreted from the posterior portion of the pituitary gland
  • Diabetes insipidus occurs in the absence of ADH; urinary output rapidly increases, causes loss of free water and severe dehydration; hypernatremia and low urine specific gravity (<1.005) [urine too diluted]
  • Tx: replacing fluid losses and ADH w/ exogenous form (IV, SubQ, intranasally)
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21
Q

Complications: Syndrome of inappropriate antidiuretic hormone (SIADH)

A

occurs when an excessive amount of ADH is secreted from the posterior pituitary

  • TBI is associated w/ disruption of the hypothalamic-pituitary axis; complication of this disruption is SIADH
  • symptoms: retention of free water; hyponatremia (dilutional); normal to low urinary output
  • Tx: restricting intake of free water: 1,000 to 2,000 mL/day
22
Q

Medical Management of TBI

A

focus on minimizing the damage caused by direct trauma to underlying brain tissue and structures, managing intracranial pressure, and promoting cerebral perfusion

  • ICP monitoring
  • Effective airway, breathing pattern, and hemodynamic stability
  • HOB elevated
  • Hyperosmolar agents to decrease fluid in the brain
23
Q

Diagnosis of TBI

A
  • Initial test: CT of the head
  • Transcranial doppler studies
  • Laboratory analysis
  • Serum sodium and osmolality
24
Q

Diagnosis: CT of head

A

initial diagnostic test performed in patients w/ traumatic head injury

25
Q

Diagnosis: Transcranial Doppler Studies

A
  • indirectly measure cerebral blood flow

- often used to determine cerebral blood cessation in severe head injuries

26
Q

Diagnosis: Laboratory studies

A
  • baseline serum electrolytes
  • complete blood cunt (CBC)
  • coagulation studies
  • serum sodium and osmolality in the event that hyperosmolar agents are used to decrease ICP
27
Q

Interventions to manage Increased ICP

A

-proper positioning
-administration of hyperosmolar agents to decrease fluid in the brain
>uncontrolled increased ICP leads to herniation syndrome

28
Q

Treatment of Herniation Syndrome

A

-“brain code”
>called brain code d/t the rapid nature of resuscitation and the resources that mirror those of cardiac arrest
-treated w/ same interventions as increased ICP to decrease ICP and relieve pressure causing displacement of brain tissue within the skull or through the foramen magnum at the bottom of the cranium

29
Q

Surgical Management of TBI

A 
-depending on type of injury
>debridement (for skull fractures)
>Cranioplasty
>Craniotomy
>Burr holes
30
Q

Surgical Management for Skull Fractures

A
  • need to debride (debridement; cleaned) and clean the wound area
  • remove any bone fragments that may be at the area of impact
  • at risk for infections of the CNS, including meningitis and encephalitis
31
Q

Surgical Management: Cranioplasty

A
  • done for displaced skull fragments d/t a displaced comminuted fracture
  • surgical repair of a bone defect in the skull
  • bone fragments are cleaned out of the brain tissue and prosthetic material is placed in the affected area of the skull
32
Q

Surgical Management: Craniotomy

A
  • for hemorrhagic injuries
  • involves opening of the skull and removal of blood accumulations
  • a surgical operation in which a bone flap is temporarily removed from the skull to access the brain
  • both epidural and subdural hematomas are surgically evacuated to decrease ICP
  • surgery not indicated w/ diffused axonal injury b/c there is no specific area of blood removal
  • after surgery, managed in the ICU, and management of ICP as priority
33
Q

Surgical Management: Burr holes

A

holes drilled in the location of the bleed to evacuate blood and relieve pressure on the brain

34
Q

Nursing Management: Assessment and Analysis

A
  • PRIORITY assessments after traumatic brain injury = monitoring for clinical manifestations of increased ICP and ensuring effective cerebral perfusion
  • BE AWARE of subtle changes in LOC (can be complicated w/ use of medications to induce barbiturate coma to decrease cerebral metabolism)
  • VITAL SIGNS: an effective blood pressure (BP) to facilitate cerebral perfusion in a patient w/ increased ICP; Glasgow Coma Scale (GCS)
35
Q

Nursing Diagnoses for TBI

A
  • Ineffective airway clearance r/t decreased LOC and inability to protect the airway
  • Ineffective cerebral tissue perfusion r/t increased ICP, cerebral edema, hemorrhage, impaired autoregulation, and hyperventilation
  • Risk for impaired skin integrity r/t bedrest, hemiparesis (weakness on one side of the body), hemiplegia (paralysis on one side of the body), immobility, decreased LOC, or restlessness
  • Impaired family coping r/t sudden life-threatening illness and uncertain outcome
36
Q

Nursing Assessments

A
  • Serial Neurological assessments q 1-2 hours in the acute phase of injury
  • Monitor for Increased ICP
  • ECG and Cardiac Biomarkers
  • Vital Signs
  • Seizure Activity
37
Q

Assessments: Serial Neurological Assessments q 1-2 hours in the acute phase of injury

A
  • continually assess the patient with a TBI against an established baseline for signs of increased ICP
  • monitor for cerebral edema, expansion of a hematoma, or conversion of a contusion to a hematoma
38
Q

Assessments: ECG and Cardiac Biomarkers

A

w/ severe TBI may demonstrate ECG findings suspicious for myocardial ischemia d/t an initial surge of catecholamines during the sympathetic nervous system response upon initial injury
-release of catecholamines during initial injury results in reversible injury to the myocardium (myocardial stunning)

39
Q

Assessments: Vital Signs

A
  • changes in vital signs are a late sign of increased ICP
  • trend BP, HR, RR, and temperature for overall condition
  • an effective BP w/ increased ICP in order to maintain a therapeutic cerebral perfusion pressure (CPP)
  • temperature elevation may be seen w/ infection (meningitis) or secondary to the area of the brain that controls thermoregulation
40
Q

Assessment: Seizure Activity

A

a TBI above the tentorium (supratentorial) and closer to the cerebral cortex are at risk for seizures b/c cellular dysfunction and tissue injury from ischemia may cause a disruption in electrical impulse conduction in the brain, causing disorganized electrical activity which is a seizure

41
Q

Nursing Actions for TBI

A
  • HOB > 30 degrees w/ head midline
  • Management of CSF leak
  • Avoid nasogastric tube placement in patients w/ known basilar skull fractures or in patients where the base of the skull has not been visualized on radiographical injury
  • Initiate enteral feeding within 72 hours
  • Maintain Normothermia
  • Seizure Precautions
  • VTE prophylaxis
42
Q

Actions: Positioning HOB greater than 30 degrees w/ head in midline; avoiding sharp hip flexion

A

facilitate drainage of venous blood from the head, decreasing ICP

43
Q

Actions: Management of CSF Leak

A
  • if clear fluid is draining from the ear or nose, it should not be stopped; collected using loosely applied gauze
  • identify a leakage of CSF b/c it indicates a break in the dura; risk for infection (meningitis, encephalitis)
  • a lumbar drain is placed when a CSF leak is persistent in order to facilitate healing of the dural tear b/c it reduces pressure on the injured tissue
  • drainage may also be tested for glucose
  • patient can also show signs of sniffling
44
Q

Actions: Avoid nasogastric tube placement in patients w/ known basilar skull fractures or in patients where the base of the skull has not been visualized on radiographical injury

A
  • may cause further disruption of a fracture
  • at risk for the tube to invade the cranium
  • orogastric tube is an alternative
45
Q

Actions: Initiate enteral tube feeding within 72 hours

A
  • starting enteral nutrition within the first 72 hours of injury in order to reach an adequate goal rate by 7 days
  • severe TBI demonstrates a hypercatabolic state where the body uses substrates at a rapid pace, causing utilization and depletion of fat and protein stores
  • bedside indirect calorimetry helpful in establishing a pts resting metabolic rate and true caloric needs to optimize nutritional regimen
  • indirect calorimetry performed by respiratory therapist or credential clinician
46
Q

Actions: Maintain Normothermic Temperature (antipyretics and cooling devices as ordered)

A

temperature maintained in order to prevent an increase in cerebral oxygen and energy demands which can worsen metabolic dysfunction in neurons

47
Q

Actions: Implement Seizure precautions

A

-have suction readily available to clear airway after a seizure
-common meds to give during a seizure: >benzodiazepines (lorazepam [Ativan]) to stop seizure activity
>antiepileptic medications (levetiracetam [Keppra] or phenytoin [Dilantin]) to prevent further seizures

48
Q

Actions: VTE prophylaxis

A
  • w/ sequential compression devices, graduated compression stocking, and subcutaneous injection of anticoagulant as prescribed
  • with severe TBI are at increased risk for VTE and subsequent pulmonary embolus b/c of tissue or endothelial damage occurring w/ the traumatic event, immobility, and hypercoagulability caused by the systemic inflammatory response that is activated after a traumatic event (Virchow’s Triad)
49
Q

Nursing Teachings

A
  • specific teaching regarding the patients injury, coma, and increased ICP
  • orientation to patients ICU room and monitoring equipment
50
Q

Urine Specific Gravity

A
  • compares the density of urine to the density of water
  • quick test can help determine how well your kidneys are diluting your urine
  • urine that’s too concentrated could mean that your kidneys aren’t functioning properly or that you aren’t drinking enough water (high)
  • normal range: 1.005- 1.030
  • high= too concentrated urine
  • low= urine too diluted

Nursing 272: Final Semester (79 decks)

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